The DOI matches its Crossref record; 46 of the 46 references it cites were found in a registry or an index; 25 of the 44 sources its claims cite were checked for support.
Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction: A Randomized, Crossover Study
Open accessAbstract
BACKGROUND: Insufficient sleep increases the risk for insulin resistance, type 2 diabetes, and obesity, suggesting that sleep restriction may impair peripheral metabolic pathways. Yet, a direct link between sleep restriction and alterations in molecular metabolic pathways in any peripheral human tissue has not been shown. OBJECTIVE: To determine whether sleep restriction results in reduced insulin sensitivity in subcutaneous fat, a peripheral tissue that plays a pivotal role in energy metabolism and balance. DESIGN: Randomized, 2-period, 2-condition, crossover clinical study. SETTING: University of Chicago Clinical Resource Center. PARTICIPANTS: Seven healthy adults (1 woman, 6 men) with a mean age of 23.7 years (SD, 3.8) and mean body mass index of 22.8 kg/m(2) (SD, 1.6). INTERVENTION: Four days of 4.5 hours in bed or 8.5 hours in bed under controlled conditions of caloric intake and physical activity. MEASUREMENTS: Adipocytes collected from subcutaneous fat biopsy samples after normal and restricted sleep conditions were exposed to incremental insulin concentrations. The ability of insulin to increase levels of phosphorylated Akt (pAkt), a crucial step in the insulin-signaling pathway, was assessed. Total Akt (tAkt) served as a loading control. The insulin concentration for the half-maximal stimulation of the pAkt-tAkt ratio was used as a measure of cellular insulin sensitivity. Total body insulin sensitivity was assessed using a frequently sampled intravenous glucose tolerance test. RESULTS: The insulin concentration for the half-maximal pAkt-tAkt response was nearly 3-fold higher (mean, 0.71 nM [SD, 0.27] vs. 0.24 nM [SD, 0.24]; P = 0.01; mean difference, 0.47 nM [SD, 0.33]; P = 0.01), and the total area under the receiver-operating characteristic curve of the pAkt-tAkt response was 30% lower (P = 0.01) during sleep restriction than during normal sleep. A reduction in total body insulin sensitivity (P = 0.02) paralleled this impaired cellular insulin sensitivity. LIMITATION: This was a single-center study with a small sample size. CONCLUSION: Sleep restriction results in an insulin-resistant state in human adipocytes. Sleep may be an important regulator of energy metabolism in peripheral tissues. PRIMARY FUNDING SOURCE: National Institutes of Health.
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Claims the paper makes
25 of 44 cited sources checked · 11 supported · 2 flagged · accuracy not yet measured
Some cited sources support this claim and some don’t — read each source’s verdict below.
In the paper
“well-controlled laboratory studies in healthy adults have shown that repeated partial sleep restriction has adverse effects on systemic insulin sensitivity and glucose tolerance”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Abstract > Primary Funding Source
What the sources say
- Disputedcites [11] sourceExperimental — accuracy not yet measured
The Results section (‘Impact of Sleep Loss on Insulin Sensitivity and Glucose Tolerance’) reports that insulin sensitivity and the response to an oral glucose load remained unchanged after four nights of sleep curtailment. The Discussion (p. 272) likewise says this short-term intervention in healthy women had no effect on basal or post-OGTT glucose metabolism, while leaving open possible long-term effects. (LLM, conf=0.88)
Checked by a reasoning model — may be wrong.
- Supportedcites [12] source
The Discussion (passages 4–5; page numbers not supplied) reports that one week of restricted sleep significantly reduced insulin sensitivity in healthy men. It also reports an earlier laboratory study in healthy subjects that found reduced glucose tolerance after repeated sleep restriction. Together, these support the citing sentence’s broad statement. (LLM, conf=0.90)
- Partly supportedcites [13] sourceExperimental — accuracy not yet measured
The Abstract reports that repeated partial sleep restriction impairs glucose tolerance, but says its effects on insulin sensitivity had not been characterized. The Discussion reports reduced insulin sensitivity after a single night of restriction in healthy subjects, not after repeated restriction. Thus the cited paper does not support the claim that repeated restriction was shown to impair both outcomes. (LLM, conf=0.89)
- Supportedcites [14] source
In “Obesity, Diabetes and Sleep Loss: Evidence from Laboratory Studies” (page not provided), the review describes controlled bedtime restriction in young adults and reports decreased insulin sensitivity and glucose tolerance after repeated short nights. It also notes consistent findings in follow-up studies. (LLM, conf=0.92)
- Not checked — no full text of the sourcecites [15] source
- Supportedcites [16] source
The Abstract describes a controlled sleep-laboratory comparison in 15 healthy men after two nights of restricted versus regular sleep. Its Conclusions report impaired glucose tolerance that appeared to be primarily caused by reduced insulin sensitivity; the Discussion likewise interprets the breakfast glucose and insulin responses as evidence of reduced insulin sensitivity. (LLM, conf=0.90)
- Not checked — no full text of the sourcecites [17] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Disputed
Some cited sources support this claim and some don’t — read each source’s verdict below.
In the paper
“To our knowledge, this finding identifies for the first time a molecular mechanism that may be involved in the reduction in total body insulin sensitivity consistently observed in multiple laboratory studies of partial sleep deprivation in healthy adults (11–17), as well as in the participants of our study.”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Discussion
What the sources say
- Disputedcites [11] sourceExperimental — accuracy not yet measured
The citation is attached to the claim that laboratory studies consistently observed reduced insulin sensitivity after partial sleep deprivation. In the paper’s “Impact of Sleep Loss on Insulin Sensitivity and Glucose Tolerance” section (p. 271), insulin sensitivity measured by both HOMA-IR and Matsuda index remained unchanged after sleep loss in healthy women. The paper therefore reports a contrary result, although it notes an association between individual changes in energy expenditure and insulin sensitivity. (LLM, conf=0.86)
Checked by a reasoning model — may be wrong.
- Supportedcites [12] source
The Discussion reports that one week of sleep restriction significantly reduced insulin sensitivity in healthy men, measured by two methods. The citation identifies this paper as one of the laboratory studies behind the sentence; the proposed molecular mechanism is the citing authors’ own finding, not a finding attributed to this source. Page numbers are unavailable in our copy. (LLM, conf=0.90)
- Supportedcites [13] source
The citation supports the reported reduction in insulin sensitivity after partial sleep deprivation in healthy adults. The Discussion reports a 19–25% reduction after one restricted night. The proposed molecular mechanism is the citing authors’ own finding, not a finding attributed to this source. (LLM, conf=0.90)
- Supportedcites [14] source
The citation supports the background finding, not the citing authors’ claim to have identified a molecular mechanism. In “Obesity, Diabetes and Sleep Loss: Evidence from Laboratory Studies,” the source reports decreased insulin sensitivity after partial sleep restriction and says several follow-up studies found consistent results; the studies involved young to middle-aged adults. (LLM, conf=0.91)
- Not checked — no full text of the sourcecites [15] source
- Supportedcites [16] source
The citation supports the reference to laboratory studies of reduced insulin sensitivity after partial sleep deprivation, not the citing authors’ claim that their own finding identifies a molecular mechanism. In the Discussion (page unavailable), Schmid et al. report that two nights of restricted sleep in healthy men produced a response pointing to reduced insulin sensitivity. The paper does not establish the citing authors’ molecular mechanism, but that is not the point attributed to this source. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites [17] source
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Disputed
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“The approximate 30% reduction in cellular insulin signaling in adipocytes induced by 4 nights of sleep restriction lies within the range of the difference in insulin sensitivity in adipocytes from obese versus lean participants (30) and from diabetic patients versus nondiabetic participants (31).”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Discussion
What the sources say
- Supportedcites [30] source
The Results (p. 1249) report lower insulin-stimulated glucose transport in adipocytes from patients with diabetes than in those from nondiabetic controls. The Results also report an approximately 40% reduction in maximal transport and a 32% reduction in maximal glucose utilization, making the cited comparison with an approximately 30% reduction reasonable. This paper is cited for the diabetic-versus-nondiabetic comparison, not for the sleep-restriction finding. (LLM, conf=0.84)
- Could not verifycites [31] sourceExperimental — accuracy not yet measured
The citation is attached to the obese-versus-lean adipocyte comparison. Our copy studies lean young subjects, and the Postmeal glucose and insulin responses section says HOMA was used to measure meal responses, not insulin sensitivity. Searches for adipocyte insulin sensitivity and obese-versus-lean differences found no passage supporting the comparison; the paper's approximately 30% figure concerns glucose tolerance and insulin response to intravenous glucose, not adipocyte signaling. (LLM, conf=0.74)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Supported
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“In all but 1 participant, the insulin-dependent response curve was shifted to the right or the maximal pAkt–tAkt ratio was decreased after sleep restriction compared with normal sleep.”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Results > Cellular Insulin Sensitivity in Adipocytes
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The total AUC of the pAkt–tAkt response to insulin was 30% lower after sleep restriction than after normal sleep (mean AUC of the pAkt–tAkt response to insulin, 893.00 [SD, 208.00] vs. 1280.00 [SD, 190.00]; mean difference, −387.00 [SD, 284.00]; P = 0.01).”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Results > Cellular Insulin Sensitivity in Adipocytes
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“The insulin concentration for the half-maximal pAkt–tAkt response was nearly 3-fold higher (mean, 0.71 nM [SD, 0.27] vs. 0.24 nM [SD, 0.24]; P = 0.01; mean difference, 0.47 nM [SD, 0.33]; P = 0.01), and the total area under the receiver-operating characteristic curve of the pAkt–tAkt response was 30% lower (P = 0.01) during sleep restriction than during normal sleep.”
- Also stated in: § Cellular Insulin Sensitivity in Adipocytes · plain
“In addition, the insulin concentration corresponding to the half-maximal pAkt–tAkt response was nearly tripled after sleep restriction than after normal sleep (0.71 nM [SD, 0.27] vs. 0.24 nM [SD, 0.24]; mean difference, 0.47 nM [SD, 0.33]; P = 0.01).”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Abstract > Results
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passes- Also stated in: § Cellular Insulin Sensitivity in Adipocytes · plain
A result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Finally, the maximum insulin-induced pAkt–tAkt response was reduced by 29% (106 [SD, 23] vs. 150 [SD, 23]; mean difference, −44 [SD, 36]; P = 0.02) during sleep restriction compared with normal sleep.”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Results > Cellular Insulin Sensitivity in Adipocytes
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Sleep restriction consistently induced a marked reduction in the pAkt response to insulin (Figure 1, right column).”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Results > Cellular Insulin Sensitivity in Adipocytes
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesA result the paper reports from its own data — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Total body insulin sensitivity was reduced by 16% after 4 days of sleep restriction compared with normal sleep (3.77 [mU/L]−1 per min−1 [SD, 1.06] vs. 3.22 [mU/L]−1 per min−1 [SD, 1.38]; mean difference, −0.58 [mU/L]−1 per min−1 [SD, 0.51]; P = 0.02).”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Results > Total Body Insulin Sensitivity
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesWhat the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“In contrast, tAkt levels did not change across study conditions or insulin concentrations (Appendix Figure).”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Results > Cellular Insulin Sensitivity in Adipocytes
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passes
- It may state two separate claims as one. 14
- Probably not a substantial claim. 10
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Insufficient sleep increases the risk for insulin resistance, type 2 diabetes, and obesity, suggesting that sleep restriction may impair peripheral metabolic pathways.”
- Also stated in: § Primary Funding Source · hedged
“prospective epidemiologic studies have found that insufficient sleep may increase the risk for metabolic disturbances, including insulin resistance, obesity, and type 2 diabetes (4–10).”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Abstract > Background
What the sources say
- Not checked — no full text of the sourcecites [4] source
- Partly supportedcites [5] sourceExperimental — accuracy not yet measured
The Results (Short duration of sleep; page not supplied) associate short sleep with a higher incidence of type 2 diabetes. The paper links reduced sleep to insulin resistance through short-term and cross-sectional studies, not prospective evidence; its Conclusions (Potential mechanisms; page not supplied) describe obesity as a possible consequence rather than a demonstrated prospective outcome. The cited evidence therefore does not support attributing all three risks to prospective studies. (LLM, conf=0.88)
- Not checked — no full text of the sourcecites [6] source
- Partly supportedcites [7] sourceExperimental — accuracy not yet measured
The Results (page unavailable) report that adults sleeping six hours or less had a higher adjusted risk of developing type 2 diabetes or impaired glucose tolerance. The Introduction and Discussion link short sleep to overweight and cite physiological evidence of insulin resistance, but this prospective study does not establish an increased risk of developing either obesity or insulin resistance. Its Discussion also cautions that a causal role for sleep curtailment remains uncertain. (LLM, conf=0.86)
- Partly supportedcites [8] sourceExperimental — accuracy not yet measured
The “Sleep and diabetes” section reports that prospective studies associate short sleep with incident diabetes, and “Sleep and BMI, obesity and appetite regulation” reports prospective associations with weight gain and childhood obesity. The paper discusses insulin resistance as a possible metabolic consequence in “Potential Mechanisms,” not as a risk established by prospective epidemiologic studies. It also cautions that observational evidence does not establish the causal claim that insufficient sleep increases these risks. Page numbers are unavailable in our copy. (LLM, conf=0.87)
- Partly supportedcites [9] sourceExperimental — accuracy not yet measured
The prospective cohort studies section reports that short sleep duration is associated with increased weight gain and obesity risk. The review does not establish increased risk of insulin resistance or type 2 diabetes; its epidemiology discussion also says a causal link between short sleep and obesity remains to be established. The citing sentence’s causal wording therefore overstates the review. (LLM, conf=0.88)
- Partly supportedcites [10] sourceExperimental — accuracy not yet measured
The Introduction (page unavailable) reports prospective evidence linking short sleep with incident type 2 diabetes and observational evidence linking inadequate sleep with obesity. The Results and Discussion (page unavailable) link short sleep to incident impaired fasting glucose and discuss insulin resistance as a possible mediator, but do not establish a higher risk of developing insulin resistance. The paper does not present prospective evidence for all three outcomes. (LLM, conf=0.88)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Also stated in: § Primary Funding Source · hedged
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“This test has been used to show an adverse effect of sleep disturbances on human glucose metabolism and insulin sensitivity in multiple previous reports (12, 15,17, 23, 24). In 1 study that used both the FSIVGTT and the euglycemic hyperinsulinemic clamp to assess changes in insulin sensitivity after experimental sleep restriction in healthy participants, both methods provided similar results (12).”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Methods > FSIVGTT
What the sources say
- Supportedcites [12] source
The Results (Insulin sensitivity and acute insulin response) report reduced insulin sensitivity and glucose tolerance after sleep restriction using the IVGTT. The Discussion explicitly says this study used both the insulin-modified FSIVGTT and the euglycemic-hyperinsulinemic clamp, with concordant results. (LLM, conf=0.94)
- Not checked — no full text of the sourcecites [15] source
- Not checked — no full text of the sourcecites [17] source
- Supportedcites [23] source
The Study Protocol says the IVGTT was performed before and after two nights of sleep fragmentation. The Results report decreases in insulin sensitivity and glucose effectiveness, supporting this paper as one of the cited reports using the test to show adverse metabolic effects. The separate comparison with a euglycemic clamp is explicitly attributed to reference 12, not to this paper. (LLM, conf=0.92)
- Not checked — no full text of the sourcecites [24] source
Strength:plain· not yet calibratedCausal:direct· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
- Supported
The cited sources that could be checked couldn’t confirm or dispute this claim.
In the paper
“Indeed, exogenous administration of cortisol or norepinephrine, 2 hormones that are hypersecreted when the hypothalamic–pituitary–adrenal axis and sympathetic nervous system are respectively activated, has been shown to induce total body (36–38) and cellular (39) insulin resistance.”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Discussion
What the sources say
- Not checked — no full text of the sourcecites [36] source
- Not checked — no full text of the sourcecites [37] source
- Not checked — no full text of the sourcecites [38] source
- Could not verifycites [39] sourceExperimental — accuracy not yet measured
The Discussion links free-fatty-acid bursts to possible obesity-related insulin resistance, but does not report that administering cortisol or norepinephrine induces insulin resistance. Searches for cortisol, norepinephrine administration, and insulin resistance found no passage establishing the claimed whole-body or cellular effect. (LLM, conf=0.76)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The sources with a verdict support this claim; the rest weren’t checked yet, have no full text we could read, or their verdicts aren’t rated yet.
In the paper
“Both reduced leptin levels (32, 33) and elevated free fatty acid concentrations (13) have been observed in healthy persons after experimental sleep restriction and could conceivably contribute to increased risk for obesity and diabetes.”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Discussion
What the sources say
- Not checked — no full text of the sourcecites [32] source
- Could not verifycites [33] sourceExperimental — accuracy not yet measured
The Discussion reports associations between self-reported sleep and cortisol secretion in the Whitehall II cohort, not an experimental sleep-restriction study. Searches of our copy for free fatty acids and leptin found no passage reporting the claimed changes in either measure. (LLM, conf=0.78)
- Supportedcites [13] source
Citation (13) is attached to the elevated free-fatty-acid finding, not the reduced-leptin finding, which cites (32, 33). The Results and Table 1 report higher nonesterified fatty acid concentrations in nine healthy subjects after sleep restriction during the hyperinsulinemic clamp (68 versus 57 µmol/L; P = 0.005); basal concentrations did not increase. (LLM, conf=0.91)
Strength:plain· not yet calibratedCausal:correlational· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
The cited sources support only part of this claim — read each source’s verdict below.
In the paper
“Further, our finding of marked alterations in adipocyte function after experimental sleep restriction challenges the widely held belief that the primary function of sleep is the restoration of central nervous system function (26–29) and suggests that sleep may play an equally important role in peripheral energy metabolism.”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Discussion
What the sources say
- Partly supportedcites [26] sourceExperimental — accuracy not yet measured
The Abstract (page unavailable) says most theories assign NREM sleep a role in nervous-system recuperation, supporting the claim that this is a common view. It also names energy conservation as a role and does not say CNS restoration is believed to be sleep’s primary function. The citation is attached to that belief, not to the citing authors’ finding about adipocytes or their conclusion about peripheral metabolism. (LLM, conf=0.82)
- Not checked — no full text of the sourcecites [27] source
- Partly supportedcites [28] sourceExperimental — accuracy not yet measured
The Background (p. 1) presents restoration of brain function as a traditional view of sleep, and the discussion of sleep homeostasis (p. 5) cites evidence that sleep reverses changes in the brain caused by wakefulness. But the paper treats whether sleep has one primary function as an open question (p. 5); it does not endorse CNS restoration as the primary function. The adipocyte finding and inference about peripheral metabolism are the citing authors’ own, not claims attributed to this source. (LLM, conf=0.82)
- Could not verifycites [29] sourceExperimental — accuracy not yet measured
The Abstract and Discussion (page numbers unavailable) address insulin signalling and glucose transport in adipocytes from obese women, not sleep. Searches for sleep restriction and restoration of central nervous system function found no passage addressing the belief to which the citation is attached. (LLM, conf=0.75)
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
- Partly supported
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Wrist activity was monitored continuously by using Actiwatch (Philips/Respironics, Andover, Massachusetts) to verify adherence to standardized bedtime schedules.”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Methods > Experimental Protocol
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“No significant changes occurred in body weight (mean body weight, 72.6 kg [SD, 10.5] under the normal sleep condition vs. 72.4 kg [SD, 9.8] under the sleep restriction condition; mean difference, 0.3 kg [SD, 1.5]; P = 0.67) or percentage of body fat (mean percentage of body fat, 22.3% [SD, 5.5%]; vs. 21.8% [SD, 5.0%]; mean difference, 0.5% [SD, 2.9%]; P = 0.66) across the entire protocol.”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Results
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes? Load-bearing: unclear✓ Based: passesIt may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Lysates collected from the same participant under both sleep conditions were simultaneously separated by sodium dodecyl sulfate polyacrylamide gel electrophoresis, then transferred to a nitrocellulose membrane. Membranes containing all samples from each participant were blocked in TBST+ (Tris-buffered saline, containing 0.1% Tween [Sigma-Aldrich], and 5% nonfat dried milk) and immunoblotted in the”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Methods > Insulin-Signaling Assay
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“This was a single-center study with a small sample size, and our sample included only 1 woman. The findings will therefore need to be replicated in a larger and more diverse population.”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Discussion
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Random assignments (ordering of the sleep conditions) were made using computer-generated random numbers and concealed with sealed envelopes.”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Methods > Experimental Protocol
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“We assessed cellular insulin sensitivity in adipocytes by examining only pAkt. Because of the limited yield of adipose tissue from our lean participants, we could not assess other components of the insulin-signaling cascade.”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Discussion
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Over the 4 nights, participants slept an average of 7.87 hours (SD, 0.31) under the normal sleep condition versus 4.35 hours (SD, 0.12) under the sleep restriction condition (mean difference, 3.53 hours [SD, 0.24]; P < 0.001).”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Results > Polysomnography
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Caloric intake was strictly controlled and identical under the 2 sleep conditions.”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Methods > Experimental Protocol
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Randomized, 2-period, 2-condition, crossover clinical study.”
- Also stated in: § Methods · plain
“Participants were tested under 2 experimental conditions in randomized order—after 4 consecutive nights of 8.5 hours in bed (normal sleep) and 4 consecutive nights of 4.5 hours in bed (sleep restriction).”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Abstract > Design
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
- Also stated in: § Methods · plain
In the paper
“Sleep was recorded by polysomnography (Neurofax EEG-1100A, Nihon Kohden, Foothill Ranch, California) each night. The recordings were visually scored in 30-second epochs as rapid eye movement (REM) sleep, non-REM sleep, and wake according to standard criteria (20).”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Methods > Experimental Protocol
What the sources say
- Not checked — no full text of the sourcecites [20] source
Load-bearingStrength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim. It may state two separate claims as one.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“The second biopsy was performed at the opposite side of the first biopsy (also within a 9-cm radius of the umbilicus) to obviate the potential effect of local inflammation on insulin sensitivity.”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Methods > Biopsy of Subcutaneous Abdominal Fat
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesProbably not a substantial claim.
What the paper did — it cites no source for this, so there is none to check. The quote shows it is in the paper.
In the paper
“Sleep restriction in our study was relatively severe and maintained over a short period of 4 days.”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Discussion
Strength:plain· not yet calibratedTests✓ Asserted: passes✓ Checkable: passes✗ Load-bearing: fails✓ Based: passesProbably not a substantial claim. The paper’s conclusions may not depend on it. It may state two separate claims as one.
A conclusion the paper draws from its own results — it cites no other source for it, so there is none to check. The quote shows it is in the paper.
In the paper
“Our findings also shed novel light on the still-elusive function of sleep, traditionally conceptualized as necessary only for the brain, because they suggest that sleep plays an important role for the functional integrity of multiple peripheral cell types, as well as for whole-body energy homeostasis.”
§ Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction > Discussion
Tests✓ Asserted: passes✓ Checkable: passes✓ Load-bearing: passes✓ Based: passesIt may state two separate claims as one.
The paper relies on this without support.
Before this study, no studies had linked sleep restriction to alterations in molecular metabolic pathways in any peripheral human tissue.
“To our knowledge, no studies to date have linked sleep restriction to alterations in molecular metabolic pathways in any peripheral human tissue.”
The paper relies on this without support.
Phosphorylation of Akt is a crucial step in the insulin-signaling pathway and a valid measure of cellular insulin sensitivity.
“The ability of insulin to increase levels of phosphorylated Akt (pAkt), a crucial step in the insulin-signaling pathway, was assessed.”
“Phosphorylation of Akt, a crucial step of the phosphatidylinositol 3-kinase (PI3K) pathway that mediates most metabolic actions of insulin, was markedly impaired after sleep restriction.”
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
In the citing paper
“Experimental sleep restriction in healthy adults results in increases in insulin resistance99 and decreases in insulin sensitivity.81”
From Sleep Duration and Quality: Impact on Lifestyle Behaviors and Cardiometabolic Health: A Scientific Statement From the American Heart Association (2016) · cites this paper as [99]
In the citing paper
“Therefore, while no changes to Glut4 mRNA or protein content were observed in tandem with changes in glucose tolerance, it is plausible that GLUT4 translocation to the cell membrane may be impaired, which would support previous research that has indicated impairments within the insulin signaling pathway following sleep restriction [52,53].”
From Exercise mitigates sleep-loss-induced changes in glucose tolerance, mitochondrial function, sarcoplasmic protein synthesis, and diurnal rhythms (2021) · cites this paper as [52]
In the citing paper
“Several well-controlled laboratory studies have consistently shown marked reductions in insulin sensitivity in young adults following sleep loss [2–7].”
From Sleep restriction increases free fatty acids in healthy men (2015) · cites this paper as [6]
In the citing paper
“Our current finding of elevated NEFA also suggests that adipocytes are resistant to the antilipolytic effects of insulin”
From Sleep restriction increases free fatty acids in healthy men (2015) · cites this paper as [6]
In the citing paper
“Sleep restriction increased the required insulin concentration to achieve half-maximal pAkt/tAkt response 3-fold, demonstrating impaired insulin signaling in abdominal fat tissue after partial sleep restriction.”
From Metabolic effects of sleep disruption, links to obesity and diabetes (2014) · cites this paper as [33]
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
Each contradiction between two passages listed here was confirmed by an independent check.
Whole-body insulin-sensitivity values conflict with the reported decline
MinorThe values are presented in the order sleep restriction versus normal sleep, which would make sensitivity higher after restriction (3.77 versus 3.22). The reported negative mean difference instead indicates a decline.
“Total body insulin sensitivity was reduced by 16% after 4 days of sleep restriction compared with normal sleep (3.77 [mU/L]−1 per min−1 [SD, 1.06] vs. 3.22 [mU/L]−1 per min−1 [SD, 1.38];”
“mean difference, −0.58 [mU/L]−1 per min−1 [SD, 0.51]; P = 0.02).”
Citations
Cites
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Impact of sleep debt on metabolic and endocrine function
Spiegel, K., Leproult, R., & Van Cauter, E. (1999) · The Lancet · doi:10.1016/s0140-6736(99)01376-8 · Cited by 3,668 · cited 2×
“This test has been used to show an adverse effect of sleep disturbances on human glucose metabolism and insulin sensitivity in multiple previous reports (12, 15, 17, 23, 24).”
BackgroundMethodReactive oxygen species have a causal role in multiple forms of insulin resistance
Houstis, N., Rosen, E. D., & Lander, E. S. (2006) · Nature · doi:10.1038/nature04634 · Cited by 2,525 · cited 1×
“Indeed, exogenous administration of cortisol or norepinephrine, 2 hormones that are hypersecreted when the hypothalamic–pituitary–adrenal axis and sympathetic nervous system are respectively activated, has been shown to induce total body (36–38) and cellular (39) insulin resistance.”
BackgroundSpiegel, K., Tasali, E., Penev, P., & Cauter, E. V. (2004) · Annals of Internal Medicine · doi:10.7326/0003-4819-141-11-200412070-00008 · Cited by 2,459 · cited 1×
“Both reduced leptin levels (32, 33) and elevated free fatty acid concentrations (13) have been observed in healthy persons after experimental sleep restriction and could conceivably contribute to increased risk for obesity and diabetes.”
BackgroundSelf-citationSleep function and synaptic homeostasis
Tononi, G., & Cirelli, C. (2006) · Sleep Medicine Reviews · doi:10.1016/j.smrv.2005.05.002 · Cited by 2,151
Sleep-dependent memory consolidation
Stickgold, R. (2005) · Nature · doi:10.1038/nature04286 · Cited by 1,857
Quantity and Quality of Sleep and Incidence of Type 2 Diabetes
Cappuccio, F. P., D'Elia, L., Strazzullo, P., & Miller, M. A. (2010) · Diabetes Care · doi:10.2337/dc09-1124 · Cited by 1,670
Short Sleep Duration and Weight Gain: A Systematic Review
Patel, S. R., & Hu, F. B. (2008) · Obesity · doi:10.1038/oby.2007.118 · Cited by 1,505
Clues to the functions of mammalian sleep
Siegel, J. M. (2005) · Nature · doi:10.1038/nature04285 · Cited by 1,040
Spiegel, K., Leproult, R., L’Hermite-Balériaux, M., Copinschi, G., Penev, P. D., & Van Cauter, E. (2004) · The Journal of Clinical Endocrinology & Metabolism · doi:10.1210/jc.2004-1003 · Cited by 1,006 · cited 1×
“Both reduced leptin levels (32, 33) and elevated free fatty acid concentrations (13) have been observed in healthy persons after experimental sleep restriction and could conceivably contribute to increased risk for obesity and diabetes.”
Background
Flagged first, then by citations
Research works printed but not linked: 2
- Leproult R, 1997, Sleep, 20, 865
- Björntorp P, 1991, Int J Obes, 15, 67
Cited by
Sorted by citations
Rosenfield, R. L., & Ehrmann, D. A. (2016) · Endocrine Reviews · doi:10.1210/er.2015-1104 · Cited by 1,603
Self-citationShort sleep duration and health outcomes: a systematic review, meta-analysis, and meta-regression
Itani, O., Jike, M., Watanabe, N., & Kaneita, Y. (2017) · Sleep Medicine · doi:10.1016/j.sleep.2016.08.006 · Cited by 1,252
“[38] Broussard JL, Ehrmann DA, Van Cauter E, Tasali E, Brady MJ.”
BackgroundSt-Onge, M.-P., Grandner, M. A., Brown, D., Conroy, M. B., Jean-Louis, G., Coons, M., & Bhatt, D. L. (2016) · Circulation · doi:10.1161/cir.0000000000000444 · Cited by 1,044
Panel, C. C., Watson, N. F., Badr, M. S., Belenky, G., Bliwise, D. L., Buxton, O. M., Buysse, D., Dinges, D. F., Gangwisch, J., Grandner, M. A., et al. (2015) · Sleep · doi:10.5665/sleep.4886 · Cited by 906
Self-citationSleep duration and risk of type 2 diabetes: a meta-analysis of prospective studies
Shan, Z., Ma, H., Xie, M., Yan, P., Guo, Y., Bao, W., Rong, Y., Jackson, C. L., Hu, F. B., & Liu, L. (2015) · Diabetes Care · doi:10.2337/dc14-2073 · Cited by 902
Metadata
- Authors
- Broussard, J. L., Ehrmann, D. A., Van Cauter, E., Tasali, E., & Brady, M. J.
- Affiliations
- University of Chicago (US)
- From the University of Chicago, Chicago, Illinois.
- Venue
- Annals of Internal Medicine
- Publisher
- American College of Physicians
- Published
- 2012-10-16
- Volume
- 157
- Issue
- 8
- Pages
- 549-557
- ISSN
- 0003-4819 (ISSN-L)
- 1539-3704
- PMC
- PMC4435718
- OpenAlex
- W2013808563
- Cited by
- 364
- References
- 46
- Citations by year
- 2026: 16 · 2025: 24 · 2024: 23 · 2023: 23 · 2022: 32 · 2021: 30 · 2020: 27 · 2019: 23 · 2018: 24 · 2017: 27 · 2016: 28 · 2015: 30 · 2014: 28 · 2013: 24 · 2012: 4
- FWCI
- 36.86
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Annals of Internal Medicine (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Georgia Clinical and Translational Science Alliance
- National Institutes of Health (DK020595, RR024999)
- National Institute on Aging (P01AG011412)
- National Heart, Lung, and Blood Institute (R01HL086459, T32HL007909)
- National Institute of Diabetes and Digestive and Kidney Diseases (P60DK020595)
- National Center for Research Resources (P41RR013642, UL1RR024999)
- Eunice Kennedy Shriver National Institute of Child Health and Human Development (P50HD057796)
- Topics
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and Work-Related Fatigue
- Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and related disorders
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adipokines, Inflammation, and Metabolic Diseases
- Keywords
- sleep restriction, insulin resistance, insulin signaling, adipocytes, subcutaneous adipose tissue, Akt phosphorylation, insulin sensitivity, energy metabolism, type 2 diabetes risk, obesity
- MeSH terms
- Adolescent, Adult, Dose-Response Relationship, Drug, Female, Glucose Tolerance Test, Humans, Insulin, Insulin Resistance, Male, Sleep Deprivation, Signal Transduction, Polysomnography, Adipocytes, Cross-Over Studies, Proto-Oncogene Proteins c-akt, Young Adult
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
A language model drew the claims from the paper on 2026-09-28, under version 3 of the claim definition (model deepseek-v4.1-flash, prompt extract-v3).
A second model labelled each claim on 2026-09-28 (model jev-1.13-20260917, definition revision gold-guideline-v0.2).
Cited sources are checked with a language model’s help (gpt-6-sol).
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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